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AKT ERK Activation - U.S. Department of Veterans Affairs

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Last Updated: 15 February 2022

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Different patterns of Akt and ERK feedback activation in response to rapamycin, active-site mTOR inhibitors and metformin in pancreatic cancer cells.

The inhibition of S6K and S6 phosphorylation induced by insulin and the GPCR agonist neurotensin is reduced by treatment of PANC-1 or MiaPaCa-2 pancreatic cancer cells with either rapamycin or active-site mTOR inhibitors here. Akt phosphorylation at Ser increased by a dramatic rise in Akt phosphorylation, but the active-site inhibitors of mTOR completely stopped Akt phosphorylation at this site. On the other hand, active-site inhibitors of mTOR promote a dramatic rise in ERK activation, while rapamycin did not have a stimulatory effect on ERK activation. The results show that the first and second generation of mTOR inhibitors can induce over-activation of various pro-oncogenic pathways in PDAC cells, indicating that closing down of feed-back loops should be a major factor in the use of these inhibitors for PDAC therapy. While all these agents potently blocked the mTORC1/S6K axis, the effects of metformin on Akt and ERK enzyme production are strikingly different from allosteric or active-site mTOR inhibitors in PDAC cells.

Source link: https://doi.org/10.1371/journal.pone.0057289

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions